This project will study the fundamental mechanism involved in acquired polymorphonuclear leukocyte (PMN) locomotory dysfunction in patients who sustained serious blunt trauma. This is important because PMN dysfunction noted in these patients is related to subsequent increased infection rate and death from sepsis. The probability that the mechanism involves: 1) release of PMN activating factors as a result of tissue damage from the trauma, 2) inappropriate activation of PMNs, 3) increased production of toxic oxygen species especially H2O2, 4)self-inflicted damage resulting from increased H2O2, and 5) dysfunction, will be investigated. Plasma from trauma patients will be tested for evidence of complement activation products C3a desArg and C5a desArg, and serum for spontaneous chemotactic activity. Lysosomal enzyme release, H2O2 production, intracellular glutathione and glutathione disulfide, and Conconavalin A capping assays will be used to prove or disprove steps 2, 3 and 4. PMN locomotory function will be assessed using a modified micropore filter assay. These assays will be performed on patients's plasma or serum specimens, and PMNs soon after trauma, 3 times a week during the first week after injury and twice in the second week. Associations between activating serum/plasma factors, biochemical cellular changes and dysfunction will be correlated by plotting and comparing resolution of abnormalities with time. If autooxidative damage is found responsible for this acquired PMN dysfunction, studies to determine the usefulness of antioxidants in these patients will be commenced.